The key points you can't miss · Anesthesiology Advanced Course 07

Chapter VI Anesthesia and Circulatory System Section 1, Heart 1, Pacing Conduction System Conduction system consists of sinoatrial node, atrioventricular node, His bundle, left and right bundle branches and Purkinje fibers
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2.
Principle of myocardial contraction The basic process of myocardial contraction: Ca2+ activates the transverse bridge between the head of the myosin molecule and the intersection of actin
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Cardiac contractility depends on: sarcoplasmic reticulum Ca2+ transport, mitochondrial ATP production and the extent of myosin ATPase activity
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3.
Cardiac output CO: The volume of blood output by the ventricle to the peripheral circulation per minute
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CO=SV*HR
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Stroke volume SV: The volume of blood delivered by the ventricle per stroke, which is the difference between the end-diastolic and end-systolic volumes of the ventricle
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Cardiac index CI=CO/body surface area, adults are about 2.
5-3.
5L/(min.
m2) Factors affecting cardiac output: venous return to the heart, peripheral vascular resistance, peripheral tissue oxygen demand, blood volume, body position, breathing pattern , heart rate, myocardial contractility
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Main factors: heart rate and stroke volume
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1.
Regulation of heart rate (1) Sympathetic nerves: through cervical sympathetic ganglia (superior, middle and inferior stellate ganglia) and cardiothoracic accelerator nerves (thoracic 1-4); (2) Parasympathetic nerves: vagus nerve distributes to sinoatrial node and atrium Ventricular node; (3) resting state parasympathetic innervation is dominant; (4) denervation, the natural rhythm of the heart, heart rate 105bpm2.
The adjustment of stroke volume determines the factors of stroke volume: preload, afterload, contractility and Abnormal activity of the ventricular wall
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(1) Preload: affected by venous system volume, ventricular compliance, intrathoracic pressure, pericardial pressure, and venous tension
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Expressed as left ventricular end-diastolic pressure LVEDP
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Under normal circumstances, PAWP ≈ LRP (left atrial pressure) ≈ LVEDP (2) afterload: the stress on the myocardial wall during the ejection of blood from the left ventricle
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It is affected by ventricular volume, wall thickness, and peripheral vascular resistance
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(3) Myocardial contractility: The intrinsic inotropic property of the myocardium is affected by intracellular calcium ion concentration and myocardial compliance
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Indicators reflecting myocardial contractility: rate of change of ventricular pressure per unit time (dP/dt), average shortening rate of myocardial fibers during ejection; cardiac pressure-volume loop; force-velocity curve,
etc.

(4) Reasons for increased cardiac output: increased heart rate (not exceeding 160bpm); increased left ventricular volume; increased return of blood to the heart; peripheral vasodilation; arteriovenous fistula; increased catecholamines
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Section II, Coronary Circulatory System I.
Anatomy (1) Composition: coronary arteries, myocardial microcirculation and venous return
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(2) The left and right coronary arteries originate from the aortic sinus near the aortic root valve
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(3) Left main: anterior descending branch: supply the anterior wall of left ventricle and right ventricle; left circumflex branch: branch to left atrium, left ventricular wall and posterior wall
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(4) Right coronary: sinoatrial node, atrioventricular node, and the posterior superior wall of the left ventricle; the posterior descending branch of the right coronary supplies the posterior wall of the left and right ventricles
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(5) The blood supply of the sinus node in 55% of people comes from the right coronary, and 45% comes from the left circumflex branch of the left coronary
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(6) Anterior cardiac vein, great cardiac vein → right atrium; smallest cardiac vein → left and right ventricle II.
Physiological (1) The increase of myocardial metabolism mainly depends on the rapid increase of coronary blood flow for compensation; (2) Adult coronary circulation blood flow.
The flow is 225ml/min, which is 4-5% of cardiac output; (3) during systole, left ventricular coronary blood flow is zero; in early diastole, 70-90% of coronary blood flow enters the myocardium
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(4) Coronary blood flow can enter the right ventricle regardless of systolic or diastolic phase
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(5) When the coronary artery is occluded, the subendocardial myocardium is easy to cause ischemia, resulting in myocardial infarction
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3.
Regulation of coronary circulation (1) Local material metabolism: the most important regulator of coronary circulation
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(1) Coronary steal: The vasodilatory substances released by the tissue in the damaged area caused by coronary stenosis first act on the normal blood vessels, because the stenotic blood vessels have reached the limit of dilation
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Coronary blood flow in normal tissue is relatively increased, while blood flow in the stenotic area is decreased
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(2) Hypoxia, dilation of coronary arteries, and decreased vascular resistance
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(2) Aortic diastolic pressure When coronary perfusion pressure is 60-150mmHg, coronary circulation has the function of automatic regulation
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(3) Left ventricular end-diastolic pressure LVEDP Coronary perfusion pressure CPP= aortic diastolic pressure DBP-left ventricular end-diastolic pressure LVEDP (4) Neural regulation Adrenaline excites cardiac α receptors and slightly constricts coronary arteries, with little effect; Beta receptors dilate coronary arteries, increasing coronary blood flow by 200%, while increasing myocardial oxygen consumption
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4.
Myocardial oxygen balance (1) Myocardium can absorb about 65% of the oxygen from coronary blood; (2) The normal value of oxygen saturation in coronary sinus is 30%; (3) The reserve function of the heart is through coronary blood (4) Factors that increase myocardial oxygen consumption: increased heart rate; increased ventricular wall tension, increased pre- and post-load; increased myocardial contractility
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(5) Reasons for reduced myocardial oxygen supply: ① Reduced coronary blood flow ② Reduced oxygen supply: anemia, hypoxia and reduction of 2,3-DPG
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(6) For heart failure or myocardial ischemia, inotropes should be used to reduce oxygen consumption of the heart
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